Beeh K M, Beier J, Kornmann O, Meier C, Taeumer T, Buhl R
Pulmonary Department, Internal Medicine, University Hospital Mainz, Mainz, Germany.
Clin Exp Allergy. 2003 Apr;33(4):475-82. doi: 10.1046/j.1365-2222.2003.01632.x.
Seasonal allergic rhinitis (SAR) is a risk factor for asthma in affected individuals. Nasal allergic inflammation enhances bone-marrow eosinophil production, mainly via IL-5, and rhinitis patients have increased airway inflammation during the pollen season.
To assess the impact of nasal allergy on sputum inflammatory markers.
In an open-labelled, randomized, placebo-controlled cross-over study with 16 non-asthmatic SAR patients (median age 25 years, 56% males), the effect of a single nasal allergen challenge performed out of season on induced sputum inflammatory parameters was evaluated. SAR patients were identified by history, skin-prick test and specific IgE. All patients had normal lung function/bronchial hyper-responsiveness out of season and a negative asthma/wheezing history. Sputum cells and supernatant levels of ECP, sICAM, IL-5 and IL-10, and plasma levels of IL-5 and ECP, were measured before and 24 h after nasal allergen challenge. After a washout period of at least 4 weeks, the procedure was repeated with placebo challenge (diluent).
Nasal allergen challenge led to an increase in sputum ECP (pre = 60 +/- 12, post = 212 +/- 63 micro g/L, P = 0.02 vs. placebo), and sICAM (4.8 +/- 2.7 to 6.5 +/- 2.9 ng/mL, P = 0.02 vs. placebo), whereas IL-10 decreased after provocation (44 +/- 11 to 29 +/- 6 pg/mL, P = 0.06 vs. placebo). Sputum IL-5 was undetectable in all patients. The absolute number of blood and sputum eosinophils did not change significantly after allergen or placebo challenge (P > 0.07, both comparisons). Plasma levels of IL-5 increased after allergen challenge (8.7 +/- 2.9 to 14.5 +/- 3.9 pg/mL, P = 0.001), and the increase in plasma IL-5 was positively correlated with the rise in sputum ECP in a subgroup of 'responders' (n = 12, r = 0.71, P = 0.01).
A single nasal allergen challenge in SAR patients increased markers of allergic inflammation in the lower respiratory tract, possibly via pronounced activation of inflammatory cells through circulating immediate-type reaction cytokines like IL-5. These findings may provide additional explanatory data for the high susceptibility of SAR patients to incident asthma.
季节性变应性鼻炎(SAR)是受累个体发生哮喘的危险因素。鼻变应性炎症主要通过白细胞介素-5(IL-5)增强骨髓嗜酸性粒细胞的生成,并且鼻炎患者在花粉季节气道炎症会加重。
评估鼻变应性炎症对痰液炎症标志物的影响。
在一项开放标签、随机、安慰剂对照的交叉研究中,对16例非哮喘性SAR患者(中位年龄25岁,56%为男性)进行了研究,评估了非花粉季节单次鼻过敏原激发对诱导痰液炎症参数的影响。通过病史、皮肤点刺试验和特异性IgE鉴定SAR患者。所有患者在非花粉季节肺功能/支气管高反应性正常,且无哮喘/喘息病史。在鼻过敏原激发前及激发后24小时测量痰液细胞以及嗜酸性粒细胞阳离子蛋白(ECP)、可溶性细胞间黏附分子(sICAM)、IL-5和IL-10的上清液水平,以及血浆中IL-5和ECP的水平。经过至少4周的洗脱期后,用安慰剂激发(稀释液)重复该操作。
鼻过敏原激发导致痰液ECP升高(激发前 = 60±12,激发后 = 212±63μg/L,与安慰剂相比P = 0.02),以及sICAM升高(4.8±2.7至6.5±2.9 ng/mL,与安慰剂相比P = 0.02),而激发后IL-10降低(44±11至29±6 pg/mL,与安慰剂相比P = 0.06)。所有患者痰液中的IL-5均未检测到。过敏原或安慰剂激发后,血液和痰液中嗜酸性粒细胞的绝对数量无显著变化(两种比较P均>0.07)。过敏原激发后血浆IL-5水平升高(8.7±2.9至14.5±3.9 pg/mL,P = 0.001),并且在一组“反应者”(n = 12)中,血浆IL-5的升高与痰液ECP的升高呈正相关(r = 0.71,P = 0.01)。
SAR患者单次鼻过敏原激发增加了下呼吸道变应性炎症标志物,可能是通过循环中的速发型反应细胞因子如IL-5显著激活炎症细胞实现的。这些发现可能为SAR患者对新发哮喘的高易感性提供更多解释性数据。